ArticleStem cells translational medicine2025
Bone mesenchymal stem cells attenuate hepatic stellate cell activation and liver fibrosis through REDD1/autophagy pathway.
Article in Stem cells translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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Who cites it
4 citing papers in PubMed.
- Vitamin A-coupled MSCs- derived extracellular vesicles relieve acute liver injury by targeting hepatic stellate cells to deliver REDD1.Journal of nanobiotechnology · 2026Article
- Novel Mechanistic Insights into Primary Biliary Cholangitis: From Pathogenesis to Mesenchymal Stem Cell-Mediated Repair.Biomedicines · 2026Review
- Sustained release of quercetin through homogeneous poly (lactic-co-glycolic acid) microspheres to enhance MSCs biofunctions for regenerative therapy.Regenerative therapy · 2026Article
- Immune cell remodelling and the peribiliary immune niche in primary biliary cholangitis: from initiation to chronicity.eGastroenterology · 2026Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
backgroundBone mesenchymal stem cells (BMSCs) have demonstrated therapeutic potential in attenuating liver fibrosis. However, the precise molecular targets through which BMSCs regulate hepatic stellate cells (HSCs) activation, as well as liver fibrosis remains unclear.
methodsBMSCs were isolated from rat bone marrow, cultured, and characterized. BMSCs were administered via tail vein injection into bile duct ligation (BDL)-induced liver fibrosis mice. The downstream target of BMSCs was analyzed using RNA-sequencing (RNA-seq) and detected in liver tissues of Primary Biliary Cholangitis (PBC) patients and mice liver fibrosis. Mechanistic evaluations were employed using immunofluorescence, Western blot, RT-qPCR, transmission electron microscope (TEM), and histological analyses.
resultsBMSCs transplantation markedly attenuated liver fibrosis. RNA-seq revealed Regulated in Development and DNA Damage Response 1 (REDD1) is a novel regulator of BMSCs-based antifibrotic liver fibrosis therapy and upregulated in liver tissues of PBC patients and mice liver fibrosis. Mechanistically, REDD1 overexpression suppressed HSCs activation by impairing HSCs autophagy, thereby potentiating BMSCs therapeutic efficacy. More importantly, the in vivo experiments revealed REDD1 treatment ameliorated liver function, alleviated liver injury, and attenuated liver fibrosis, and PI3K/AKT/mTOR and TGFβ/Smad3 pathway were involved in the regulation.
conclusionsOur results provide preliminary evidence for the protective roles of BMSCs in liver fibrosis through REDD1/autophagy pathway and suggest that REDD1 may be a promising therapeutic target for treating liver fibrosis.
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